ReviewThe Journal of physiology2012
Ca2+/calmodulin-dependent protein kinase II function in vascular remodelling.
Review in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 44 citations in OpenAlex.
- Calcium Signaling Dynamics in Vascular Cells and Their Dysregulation in Vascular Disease.Biomolecules · 2025Review
- CPS1 augments hepatic glucagon response through CaMKII/FOXO1 pathway.Frontiers in pharmacology · 2024Article
- CaMKII Splice Variants in Vascular Smooth Muscle Cells: The Next Step or Redundancy?International journal of molecular sciences · 2022Review
- CaMKIIδ is upregulated by pro-inflammatory cytokine IL-6 in a JAK/STAT3-dependent manner to promote angiogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Interactive Roles of CaMKII/Ryanodine Receptor Signaling and Inflammation in Lung Diseases.Advances in experimental medicine and biology · 2021Review
- Systematic Understanding of Pathophysiological Mechanisms of Oxidative Stress-Related Conditions-Diabetes Mellitus, Cardiovascular Diseases, and Ischemia-Reperfusion Injury.Frontiers in cardiovascular medicine · 2021Review
- Enhanced KCl-mediated contractility and CaAmerican journal of physiology. Heart and circulatory physiology · 2020Article
- Canonical transient receptor potential 6 channel deficiency promotes smooth muscle cells dedifferentiation and increased proliferation after arterial injury.JVS-vascular science · 2020Article
- Thymine DNA glycosylase is a key regulator of CaMKIIγ expression and vascular smooth muscle phenotype.American journal of physiology. Heart and circulatory physiology · 2019Article
- Elucidating the contributory role of microRNA to cardiovascular diseases (a review).Vascular pharmacology · 2019Review
- Expression profiles of circRNAs and the potential diagnostic value of serum circMARK3 in human acute Stanford type A aortic dissection.PloS one · 2019Article
- MerTK signaling in macrophages promotes the synthesis of inflammation resolution mediators by suppressing CaMKII activity.Science signaling · 2018Article
- Calcium/calmodulin-dependent kinase 2 mediates Epac-induced spontaneous transient outward currents in rat vascular smooth muscle.The Journal of physiology · 2017Article
- Chronic hypoxia alters fetal cerebrovascular responses to endothelin-1.American journal of physiology. Cell physiology · 2017Article
- MicroRNA-30 inhibits neointimal hyperplasia by targeting Ca(2+)/calmodulin-dependent protein kinase IIδ (CaMKIIδ).Scientific reports · 2016Article
- Mechanisms of Vascular Smooth Muscle Contraction and the Basis for Pharmacologic Treatment of Smooth Muscle Disorders.Pharmacological reviews · 2016Review
- Ca2+/calmodulin-dependent protein kinase II-γ (CaMKIIγ) negatively regulates vascular smooth muscle cell proliferation and vascular remodeling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Review
- Transient receptor potential channels in the vasculature.Physiological reviews · 2015Review
- Resistance to aerobic exercise training causes metabolic dysfunction and reveals novel exercise-regulated signaling networks.Diabetes · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Vascular smooth muscle (VSM) undergoes a phenotypic switch in response to injury, a process that contributes to pathophysiological vascular wall remodelling. VSM phenotype switching is a consequence of changes in gene expression, including an array of ion channels and pumps affecting spatiotemporal features of intracellular Ca(2+) signals. Ca(2+) signalling promotes vascular wall remodelling by regulating cell proliferation, motility, and/or VSM gene transcription, although the mechanisms are not clear. In this review, the functions of multifunctional Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) in VSM phenotype switching and synthetic phenotype function are considered. CaMKII isozymes have complex structural and autoregulatory properties. Vascular injury in vivo results in rapid changes in CaMKII isoform expression with reduced expression of CaMKIIγ and upregulation of CaMKIIδ in medial wall VSM. SiRNA-mediated suppression of CaMKIIδ or gene deletion attenuates VSM proliferation and consequent neointimal formation. In vitro studies support functions for CaMKII in the regulation of cell proliferation, motility and gene expression via phosphorylation of CREB1 and HDACIIa/MEF2 complexes. These studies support the concept, and provide potential mechanisms, whereby Ca(2+) signalling through CaMKIIδ promotes VSM phenotype transitions and vascular remodelling.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.